Ch 11 Flashcards
What is normal microbiota?
permanently colonize the host and either cause no harm to the host or are beneficial to their host
transient microbiota
may be present for days, weeks, or months, more easily lost but are not harmful to the host
types of symbiosis
commensalism
one organism benefits
other is unaffected
types of symbiosis
mutualism
both organisms benefit
types of symbiosis
parasitism
one organism benefits and the expense of the other
How can normal flora cause disease?
Cause disease when in a new area of the body or host is immunocompromised aka opportunistic pathogens
Ex ecoli UTIs
primary infections
Acute infection that causes the
initial illness
secondary infections
Opportunistic infection after a
primary (predisposing) infection
Know a few factors that make us predisposed to disease
age
lifestyle
fatigue
What is a reservoir?
Continual sources of infection; living or nonliving
examples of reservoirs
humans
AIDS, gonorrhea
carriers may have subclincal (unapparent) infections or latent diseases
example of reservoirs
animals/ insects
rabies, lyme disease
zoonoses may be transmitted to humans from non-human reservoirs
examples of reservoirs
nonliving/ abiotic
botulism, tetanus
spores of clostridium species are found in soil and water
What are the 3 main routes of transmission?
direct
indirect
contact
direct transmission
droplet (aerosol)
body fluid exchange
fecal-oral
contact (STDs)
indirect transmission
foodborne
water-borne
fomite (inantimate object contact)
insect vectors/ animal zoonoses
environmental
contact transmission
direct: with infected/ reservoir
indirect: with inanimate object as intermediate
congenital: mother to fetus or to newborn at birth
What is a fomite?
indirect transmission
carry infectious microbes between hosts
ex. hypodermic syringe
transmission of arthropods
mechanical
arthropod carries pathogen on feet to host
host causes further contamination to self
transmission of arthropods
biological
pathogen reproduces in vector (insect) and is injected when insect bites host
What is MRSA?
methicillin resistant Staphylococcus aureus
resistant to the broad-spectrum antibiotics commonly used to treat it; can be fatal
mostly occurs in hospital aka healthcare-associated (MRSA or HA-MRSA)
older adults and people with weakened immune systems are at most risk of HA-MRSA
What are some factors that contribute to emerging and reemerging diseases?
genetic recombination
inappropriate use of antibiotics and pesticides
evolution of new strains
3 basic types of epidemiology.
descriptive
analytical
experimental
types of epidemiology
descriptive
collection and analysis of data
john snow
types of epidemiology
analytical
comparison of a diseased group and a healthy group
nightingale23e4
types of epidemiology
experimental
controlled experiments to learn how to prevent the spread of disease
What are features and examples of nosocomial infections?
aka healthcare associated infections
acquired during a hospital stay
affects 5-15% of all patients
reduced by following proper aseptic techniques during patient care and procedures
examples of nosocomial infections aka healthcare associated infections
Urinary tract infections (UTIs)
surgical site infections
lower respiratory infections
In what ways can opportunistic bacteria cause disease?
causes disease when in new area of body OR host is immunocompromised
ex e coli UTIs
Know all terms involved in pathogenicity, virulence, and toxicity
3 main characteristics of pathogens that determine virulence
infectivity
ability to establish focal point of infection
** 3 main characteristics of pathogens that determine virulence**
invasiveness
ability to spread to adjacent tissues
3 main characteristics of pathogens that determine virulence
pathogenic potential
degree to which potential can cause damage to host
What are the 3 main routes of entry into the body?
mucous membranes
skin
oral-fecal route
ID50
infectious dose for 50% of the test population
the amount of pathogen it takes for 1/2 of the individuals tested to become infected
LD50
lethal dose (of a toxin) for 50% of the test population
the amount of toxin required to kill 1/2 of the individuals tested
Do microorganisms have a preferred portal of entry? What does that mean?
most pathogens do have a preferred portal of entry
the portal of entry determines how many spores the bacteria will produce which will show how many bacteria are required to establish infection
What are adhesins?
bind to receptors on host cells-INVASION
ex of adhesions
glycocalyx: Streptococcus mutans
fimbriae: Escherichia coli
M protein: Streptococcus pyogenes
What are some ways in which pathogenic bacteria have evolved ways to get around the immune system
cell wall: evasion
capsules: cover surface markers in their cell walls
enzymes: evasion and damage
hemolysins: lyse RBCs to release iron for pathogen use
exotoxin
gram pos
proteins with 2 subunits (A-B)
heat unstability b/c these are proteins high temp denatures them
high toxicity
neutralized by antitoxin
small lethal dose
endotoxin
gram neg
lipid
heat stability b/c high temp does not kill lipids
low toxicity
not easily neutralized by antitoxin
larger lethal does
exotoxin
A subunit
B subunit
A subunit
does the damage / is toxic to the host cell
B subunit
extoxin is responsible for binding it to the target cell and transporting the A subunit into the target cell
What are the general steps of entry of an A-B exotoxin?
- bacterium produces and releases exotoxin
- B (binding) component of exotoxin attaches to host cell receptor
- A-B exotoxin enters host cell by endocytosis
- A-B exotoxin enclosed in pinched-off portion of plasma membrane during pinocytosis
- A-B components of exotoxin seperate
The A component alters cell function by inhibiting protein synthesis
The B component is released from the host cell
membrane-disrupting exotoxins
Lyse host cells by making protein channels in the
host cell membranes
What are superantigens
cause an intense immune response
due to a massive release of cytokines from host cells
- Intense immune response occurs because they activate
more immune cells than normal by binding non-
specificall
stages of disease
- incubation period
time between infection with a
microbe and the onset of
symptoms
stages of disease
- prodromal period
first appearance of mild or nonspecific signs and symptoms of an illness
stages of disease
- acute illness
most severe signs and symptoms
stages of disease
- convalescence
the recovery period after an illness
infection
invasion and growth of bacteria
intoxication
Disease that results from a specific
toxin which may or may not have been produced
during the infection (some toxin are very stable!
capsules: evasion
pathogens can avoid detection by host phagocytes by
covering surface markers on their cell walls
capsules: evasion
is used by
Streptococcus pneumoniae, Bacillus anthracis Haemophilus influenzae
capsules:evasion
Otherwise host phagocytes recognize pathogen cell
markers with receptors on their surfaces
Bacterial markers and host phagocyte receptors
interact to initiate phagocytosis
- Once ingested: Lysosomes use a complex mixture of
digestive enzymes and destructive oxygen radicals
(e.g. super oxides) to destroy pathogens
process of phagocytosis
- chemotaxis and adherence of microbe to phagocyte
- ingestion of microbe by phagocyte
- formation of a phagosome
- fusion of the phagosome with a lysosome to form a phagolysosome
- digestion of ingested microbe by enzymes
- formation of residual body containing indigestible material
- discharge of waste materials
cell wall components: evasion
Many pathogenic bacteria have cell wall
factors that help
them evade the host’s immune system
cell wall components: evasion
M protein
in Streptococcus pyogenes (also used in
adherence to host cells) helps resist phagocytosis
cell wall components: evasion
Opa proteins
inhibits interactions between Neisseria
gonorrhoeae and T helper cells due to very tight packing
between bacterial cells mediated by Opa proteins
cell wall components: evasion
mycolic acids
in (acid fast bacteria) Mycobacterium
tuberculosis and Mycobacterium leprae make it difficult
for phagocyte lysozomes to digest/destroy the pathogen
enzymes: evasion and damage
some pathogenic bacteria produce enzymes that help them establish
an infection and/or cause damage to their host
enzymes: evasion and damage
Coagulase
causes clotting of the blood; converts fibrinogen to fibrin which
coats the bacteria to help it evade phagocyte detection
enzymes: evasion and damage
Kinases
ex. streptokinase
digests fibrin clots which allow pathogens to
escape from a clot and spread
enzymes: evasion and damage
Hyaluronidase
hydrolyzes hyaluronic acid which helps hold cells together,
allowing easy spread in host tissues
enzymes: evasion and damage
Collagenase
hydrolyzes collagen to allow pathogen to spread in
connective tissues
enzymes: evasion and damage
IgA protease
destroys IgA antibodies produced by the host
enzymes: evasion and damage
Hemolysins
lyse red blood cells to release iron for pathogen use
